The long-term objective is to describe the effect that composition of dietary fat has on prostaglandin metabolism in the rat. Many tissues show an opposite response when comparing the F vs E series or one vs two series of protaglandins. Dietary linoleate is converted to precursors of prostaglandins, but, if stored directly in tissues and then released, linoleate inhibits prostaglandin synthesis. Ex vivo production of prostaglandins F2 alpha, E2 and E1 by platelets (serum), heart, lung, liver, kidney medulla and adipocytes has been validated. Aspirin was used to stop prostaglandin synthesis and the specified prostaglandins were determined by radioimmunoassay. An increase in degree of polyunsaturation of dietary fat significantly enchanced ex vivo prostaglandin production by platelets, liver and adipocytes. Only minor changes in prostaglandin ratios were observed. No effect on platelet clotting time nor adipocyte lipolysis--physiological responses that are affected by prostaglandins--was noted. The composition of the fatty acids in tissue phospholipids, which are the precursors of prostaglandins, is being assayed. Antibodies will be raised to prostaglandin serum and urinary metabolities and recently discovered thromboxane B2. Plasma and urinary levels of the former should reflect the total body production of prostaglandins. Ex vivo production of thromboxane will be investigated by repeating the above research designs. Liver glycogenolysis is stimulated by prostaglandin E1 but not F2 alpha nor E2. It will be used an an indirect assay of prostaglandin E1 production. The quantitative relationships between these parameters and composition of dietary fat will be investigated. Other nutrients, such as, antioxidants and selenium, might be involved in altering the prostaglandins and they will be tested. Evidence suggests that antioxidants inhibit prostaglandin synthesis, in vitro.